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行走患者类骨质厚度和矿化延迟时间的季节性变化。

Seasonal change in osteoid thickness and mineralization lag time in ambulant patients.

作者信息

Need Allan G, Horowitz Michael, Morris Howard A, Moore Robert, Nordin Christopher

机构信息

Institute of Medical and Veterinary Science, Adelaide, South Australia, Australia.

出版信息

J Bone Miner Res. 2007 May;22(5):757-61. doi: 10.1359/jbmr.070203.

Abstract

UNLABELLED

Low vitamin D levels are common. Bone biopsies taken from 121 ambulant patients were therefore reviewed. Seasonal changes in mineralization correlated inversely with serum 25-hydroxyvitamin D but not the more active metabolite, 1,25-dihydroxyvitamin D. This implies that the latter is produced in bone.

INTRODUCTION

It has been 30 yr since a seasonal variation in osteoid surfaces and calcification fronts was noted in bone biopsies from hip fracture patients in Leeds and attributed to vitamin D status. It was suggested at that time that mild vitamin D deficiency might cause osteoporosis from malabsorption of calcium and more severe deficiency osteomalacia, but little has been published on this subject since.

MATERIALS AND METHODS

We examined bone biopsies, calcium absorption data, and serum vitamin D metabolites in 121 patients attending our osteoporosis clinics in Adelaide. Biopsies were collected from the anterior iliac crest with a Jamshidi needle after two stat oral doses of 1 g of tetracycline 10 days apart, processed into plastic without demineralization, and all parameters were measured by point counting using a Weibel II graticule. Calcium absorption was measured after an oral dose of 5 microCi of (45)Ca in 250 ml of water with 20 mg of calcium carrier. Serum 25-hydroxyvitamin D [25(OH)D] was measured by radioimmunoassay and 1,25-dihydroxyvitamin D [1,25(OH)(2)D] by radioimmunoassay after high-performance liquid chromatography (HPLC).

RESULTS

25(OH)D levels were lower from late autumn to early spring (April to September) than from late spring to early autumn (October to March) (51 +/- 23 versus 61 +/- 27 [SD] nM; p=0.040). None of the biopsies yielded a diagnosis of osteomalacia, but osteoid thickness (O.Th.) was greater in the winter than the summer months (8.5 +/- 3.6 versus 7.1 +/- 2.8 microm; p=0.015) as was mineralization lag time (MLT; 11.9 +/- 5.2 versus 9.5 +/- 3.6; p=0.005). O.Th and log MLT were both inversely related to serum 25(OH)D (p=0.014 and 0.036) but not serum 1,25(OH)(2)D. Calcium absorption was related to serum 1,25(OH)(2)D but not serum 25(OH)D.

CONCLUSIONS

We conclude that circulating 25(OH)D affects the mineralization process, whereas circulating 1,25(OH)(2)D affects bone indirectly through its effect on calcium absorption.

摘要

未标注

维生素D水平低很常见。因此,对121名门诊患者的骨活检进行了回顾。矿化的季节性变化与血清25-羟基维生素D呈负相关,但与活性更高的代谢物1,25-二羟基维生素D无关。这意味着后者是在骨骼中产生的。

引言

自利兹髋部骨折患者的骨活检中发现类骨质表面和钙化前沿的季节性变化并归因于维生素D状态以来,已经过去了30年。当时有人提出,轻度维生素D缺乏可能因钙吸收不良导致骨质疏松,而更严重的缺乏则导致骨软化症,但此后关于这个主题的报道很少。

材料与方法

我们检查了阿德莱德骨质疏松门诊的121名患者的骨活检、钙吸收数据和血清维生素D代谢物。在口服两次间隔10天的1克四环素后,用Jamshidi针从髂前嵴采集活检样本,不经脱矿处理制成塑料切片,所有参数均使用Weibel II网格通过点计数法测量。口服250毫升含20毫克钙载体的水中5微居里的(45)钙后测量钙吸收。血清25-羟基维生素D [25(OH)D]通过放射免疫测定法测量,1,25-二羟基维生素D [1,25(OH)2D]在高效液相色谱(HPLC)后通过放射免疫测定法测量。

结果

从深秋到早春(4月至9月)的25(OH)D水平低于晚春到初秋(10月至3月)(51±23与61±27 [标准差] nM;p = 0.040)。没有一份活检诊断为骨软化症,但冬季的类骨质厚度(O.Th.)大于夏季(8.5±3.6与7.1±2.8微米;p = 0.015),矿化延迟时间(MLT)也是如此(11.9±- 5.2与9.5±3.6;p = 0.005)。O.Th和log MLT均与血清25(OH)D呈负相关(p = 0.014和0.036),但与血清1,25(OH)2D无关。钙吸收与血清1,25(OH)2D有关,但与血清25(OH)D无关。

结论

我们得出结论,循环中的25(OH)D影响矿化过程,而循环中的1,25(OH)2D通过其对钙吸收的影响间接影响骨骼。

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